The studies on cerebral ischemia, its pathophysiology, prevention and therapy in gerbils have been concerned with continuous evaluation of the effects of naturally occurring central nervous system depressant [Gamma-butyrolactone (GBL) and Gamma-hydroxybutyrate (GHB)] on cerebral ischemia focusing on the elucidation of the possible mechanisms responsible for the observed beneficial effect of GBL and GBH on ischemic brain edema. These investigations showed that the postischemic GHB treatment 3 hours after release of bilateral carotid occlusion markedly reduced the ischemically accumulated tryptophan (the precursor of 5HT), raised significantly the level of 5HT and normalized 5-HIAA concentration in the cortex, hippocampus and striatum as compared to the respective values found at 4 hours of reflow in untreated gerbils. These findings indicate that the postischemic GHB treatment stabilizes the ischemically disturbed serotonin metabolism. Therefore, the observed short term improvement in the metabolism of one of the monoamines following a relatively late postischemic treatment warrants further studies of GHB as a potential therapeutic agent in cerebral ischemia.